Asymmetric dimethylarginine: a key player in the pathophysiology of endothelial dysfunction, vascular inflammation and atherosclerosis in rheumatoid arthritis?

2021 ◽  
Vol 27 ◽  
Author(s):  
Arduino A Mangoni ◽  
Sara Tommasi ◽  
Salvatore Sotgia ◽  
Angelo Zinellu ◽  
Panagiotis Paliogiannis ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Endothelial Dysfunction ◽  
Asymmetric Dimethylarginine ◽  
Vascular Inflammation ◽  
Good Evidence ◽  
Plaque Deposition ◽  
Pathophysiological Role ◽  
Autoimmune Condition ◽  
And Oxidative Stress

: Patients with rheumatoid arthritis (RA), a chronic and disabling autoimmune condition that is characterized by articular and extra-articular manifestations and a pro-inflammatory and pro-oxidant state, suffer from premature atherosclerosis and excessive cardiovascular disease burden. A key step in the pathogenesis of atherosclerosis is the impaired synthesis of the endogenous messenger nitric oxide (NO) by endothelial cells which, in turn, alters local homeostatic mechanisms and favors vascular damage and plaque deposition. While the exact mechanisms of endothelial dysfunction in RA remain to be established, there is good evidence that RA patients have relatively high circulating concentrations of the methylated arginine asymmetric dimethylarginine (ADMA), a potent endogenous inhibitor of endothelial NO synthase (eNOS). This review discusses the biological and pathophysiological role of ADMA, the interplay between ADMA, inflammation and oxidative stress, and the available evidence on the adverse impact of ADMA on endothelial function and atherosclerosis and potential ADMA-lowering therapies in RA patients.

scholarly journals Pathophysiological Role of Adiponectin, Leptin and Asymmetric Dimethylarginine in the Process of Atherosclerosis

Folia Medica ◽  
2016 ◽  
Vol 58 (4) ◽  
pp. 234-240 ◽  
Author(s):  
Daniela Iv. Koleva ◽  
Maria M. Orbetzova ◽  
Julia G. Nikolova ◽  
Tanya I. Deneva
Keyword(s):  
Cardiovascular Disease ◽  
Adipose Tissue ◽  
Endothelial Dysfunction ◽  
Proinflammatory Cytokines ◽  
Asymmetric Dimethylarginine ◽  
Serum Levels ◽  
Reactive Protein ◽  
Proinflammatory Mediators ◽  
Pathophysiological Role

Abstract Adipose tissue is recognized as a rich source of proinflammatory mediators that may directly contribute to vascular injury, insulin resistance, and atherogenesis. Many studies have shown that adiponectin has antiatherogenic and anti-inflammatory properties. Adiponectin acts not only as a factor increasing insulin sensitivity, and the protective effect may result from its ability to suppress production of proinflammatory cytokines. It negatively regulates the expression of TNF-alpha and C-reactive protein (CRP) in adipose tissue; reduces expression of vascular and intracellular adhesion molecules (VCAM-1, ICAM-1), E-selectin, interleukin-8 (IL-8). Hyperleptinemia has been linked with the development of hypertension and endothelial dysfunction/atherosclerosis, two main pathophysiological conditions associated with cardiovascular disease development. Leptin-mediated increases in sympathetic nervous system activity may be among the principal mechanisms evoking obesity related hypertension. Leptin stimulates the secretion of proinflammatory cytokines, and increases the release of endothelin-1 (ET-1), which may promote hypertension. Increased serum levels of asymmetric dimethylarginine (ADMA), a physiological regulator of the biosynthesis of nitric oxide (NO), promote the process of atherosclerosis, leading to the occurrence of endothelial dysfunction and cardiovascular disease.

AB0133 Role of Monocytes Subsets in the Atherothrombosis and Endothelial Dysfunction Associated with Rheumatoid Arthritis: Beneficial Effects of Tocilizumab

2015 ◽  
Vol 74 (Suppl 2) ◽  
pp. 935.2-935
Author(s):  
N. Barbarroja ◽  
P. Ruiz-Limon ◽  
C. Perez-Sanchez ◽  
Y. Jimenez-Gomez ◽  
M. Abalos-Aguilera ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Endothelial Dysfunction ◽  
Beneficial Effects

Abstract 357: Hepatic ERK2 Suppresses Endoplasmic Reticulum Stress, Leading to Protection from Oxidative Stress and Endothelial Dysfunction

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Takehiko Kujiraoka ◽  
Yasushi Satoh ◽  
Makoto Ayaori ◽  
Yasunaga Shiraishi ◽  
Yuko Arai-Nakaya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Endoplasmic Reticulum ◽  
Fatty Acid ◽  
Endothelial Dysfunction ◽  
Er Stress ◽  
Vascular Complications ◽  
Metabolic Remodeling ◽  
And Oxidative Stress

Background Insulin signaling comprises 2 major cascades, the IRS/PI3K/Akt and Ras/Raf/MEK/ERK pathways. Many studies on the tissue-specific effects of the former pathway had been conducted, however, the role of the latter cascade in tissue-specific insulin resistance had not been investigated. High glucose/fatty acid toxicity, inflammation and oxidative stress, all of which are associated with insulin resistance, can activate ERK. Liver plays a central role of metabolism and hepatosteatosis (HST) is associated with vascular diseases. The aim of this study is to elucidate the role of hepatic ERK2 in HST, metabolic remodeling and endothelial dysfunction. Methods Serum biomarkers of vascular complications in human were compared between subjects with and without HST diagnosed by echography for regular medical checkup. Next, we created liver-specific ERK2 knockout mice (LE2KO) and fed them with a high-fat/high-sucrose diet (HFHSD) for 20 weeks. The histological analysis, the expression of hepatic sarco/endoplasmic reticulum (ER) Ca 2+ -ATPase 2 (SERCA2) and glucose-tolerance/insulin-sensitivity (GT/IS) were tested. Vascular superoxide production and endothelial function were evaluated with dihydroethidium staining and isometric tension measurement of aorta. Results The presence of HST significantly increased HOMA-IR, an indicator of insulin resistance or atherosclerotic index in human. HFHSD-fed LE2KO revealed a marked exacerbation in HST and metabolic remodeling represented by the impairment of GT/IS, elevated serum free fatty acid and hyperhomocysteinemia without changes in body weight, blood pressure and serum cholesterol/triglyceride levels. In the HFHSD-fed LE2KO, mRNA and protein expressions of hepatic SERCA2 were significantly decreased, which resulted in hepatic ER stress. Induction of vascular superoxide production and remarkable endothelial dysfunction were also observed in them. Conclusions Hepatic ERK2 revealed the suppression of hepatic ER stress and HST in vivo , which resulted in protection from vascular oxidative stress and endothelial dysfunction. HST with hepatic ER stress can be a prominent risk of vascular complications by metabolic remodeling and oxidative stress in obese-related diseases.

scholarly journals Concentrations of the Selected Biomarkers of Endothelial Dysfunction in Response to Antiepileptic Drugs: A Literature Review

2019 ◽  
Vol 25 ◽  
pp. 107602961985942 ◽  
Author(s):  
Beata Sarecka-Hujar ◽  
Izabela Szołtysek-Bołdys ◽  
Ilona Kopyta ◽  
Barbara Dolińska ◽  
Andrzej Sobczak
Keyword(s):  
Risk Factors ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Literature Review ◽  
Antiepileptic Drug ◽  
Asymmetric Dimethylarginine ◽  
The Body ◽  
Biochemical Processes ◽  
The Brain

Epilepsy is a disease arising from morphological and metabolic changes in the brain. Approximately 60% of patients with seizures can be controlled with 1 antiepileptic drug (AED), while in others, polytherapy is required. The AED treatment affects a number of biochemical processes in the body, including increasing the risk of cardiovascular diseases (CVDs). It is indicated that the duration of AED therapy with some AEDs significantly accelerates the process of atherosclerosis. Most of AEDs increase levels of homocysteine (HCys) as well as may affect concentrations of new, nonclassical risk factors for atherosclerosis, that is, asymmetric dimethylarginine (ADMA) and homoarginine (hArg). Because of the role of these parameters in the pathogenesis of CVD, knowledge of HCys, ADMA, and hArg concentrations in patients with epilepsia treated with AED, both pediatric and adult, appears to be of significant importance.

Predictors of asymmetric dimethylarginine levels in patients with rheumatoid arthritis: the role of insulin resistance

2013 ◽  
Vol 42 (3) ◽  
pp. 176-181 ◽  
Author(s):  
T Dimitroulas ◽  
A Sandoo ◽  
JJJCS Veldhuijzen van Zanten ◽  
JP Smith ◽  
J Hodson ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Insulin Resistance ◽  
Asymmetric Dimethylarginine

scholarly journals A psoriasis és az oxidatív stressz

2016 ◽  
Vol 157 (45) ◽  
pp. 1781-1785 ◽  
Author(s):  
Iván Péter ◽  
Anna Jagicza ◽  
Zénó Ajtay ◽  
István Kiss ◽  
Balázs Németh
Keyword(s):  
Oxidative Stress ◽  
Asymmetric Dimethylarginine ◽  
Joint Damage ◽  
Cancer Genetic ◽  
Endogenous Factors ◽  
Increased Risk ◽  
Inflammatory Bowel ◽  
And Oxidative Stress

Psoriasis is among the most common dermatological diseases worldwide. Its significance is emphasized by adverse effects on quality of life, caused by chronic pain, physical and psychical disability due to psoriatic plaques. Besides the development of psoriatic arthritis, which often causes permanent joint damage, former studies revealed an increased risk of inflammatory bowel disease, cardiovascular disease and certain types of cancer. Genetic predisposition and oxidative stress caused by exogenous and endogenous factors can contribute to abnormal differentiation and hyperproliferation of keratinocytes, accordingly the development and maintenance of psoriasis. Moreover, excessive oxidative stress can be responsible for the onset of psoriasis complications. After a brief pathophysiological summary the authors discuss the role of oxidative stress in the development of psoriasis and its complications through several well studied biomarkers (asymmetric dimethylarginine, malondialdehyde, superoxide dismutase, catalase). Orv. Hetil., 2016, 157(45), 1781–1785.

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